Abstrait

Neurological manifestations of corona virus infection

Alina

Corona virus is a single-stranded neurotropic RNA virus and it enters into the brain through the olfactory bulb following nasopharyngeal exposure. The Angiotensin converting enzyme 2 receptor (ACE-2), to which SARS-CoV-2 binds for entry into cells, found in brain vascular endothelium and smooth muscle and SARS-CoV-2 replicates in neuronal cells. It causes oedema, neuronal necrosis, and broad gliocyte hyperplasia. The elevated expression of the cytokine, monokine induced by gamma interferon (known as MIG or CXCL9), and with infiltration of monocytes and macrophages plus T cells are consistent with viral CNS entry, triggering the release of cytokines and chemokines, which contribute to tissue damage. A vasculitis process similar to that for varicella zoster virus, in which viral replication in the cerebral arterial wall triggers local inflammation, endothelial infection by SARS-CoV-2 and stroke are consistent with a virus-associated microangiopathic process. Competitive blockage of angiotensin-converting enzyme 2 by the SARS-CoV-2 virus down-regulates angiotensin-converting enzyme 2 expression leading to uncontrolled blood pressure and the enhanced possibility of cerebrovascular accidents. The SARS-CoV-2 virus epitopes bear a structural resemblance to several human proteins. Molecular mimicry between virus epitope and myelin basic protein results in autoimmune postinfectious demyelinating syndromes. Spike surface glycoprotein plays a crucial role in immunopathology. Dysregulation of the angiotensin-converting enzyme 2 receptor contributes to the pathogenesis of experimental autoimmune encephalomyelitis. Guillain-Barré syndrome is a frequently encountered neurological complication of COVID-19. Zhao and co-workers described the first patient of Guillain-Barré syndrome in a patient with COVID-19. After this, 18 more patients of Guillain-Barré syndrome in COVID-19, have been described. Miller Fisher syndrome is a variant of Guillain-Barré syndrome and is characterized by ophthalmoplegia, ataxia, and areflexia. Has also been described in patients with Covid-19. Treatment with intravenous immunoglobulins lead to complete or partial recovery in the majority. A serine protease enzyme inhibitor blocks viral entry into the host cell. This phenomenon can be exploited for developing a treatment of COVID-19, in the future.